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If there is not a match of indexes that identify query results, a full table scan occurs. When dealing with large data warehouse tables, a large volume of data could be sent to the database server, where subsequent determination of the query results occurs prior to returning the results to the business analyst. Return of such large data volumes from storage to database server nodes through limited bandwidth is the reason that many poorly performing Oracle data warehouses are said to be throughput-bound. In comparison, where Exadata storage is present and Smart Scans are used, the database server kernel is Exadata aware. In reality, there is constant modulation between database processes and the Exadata Storage Server cells, but to provide you with a simplified explanation and diagram, we show an iDB command sent to the Exadata Storage Server cells in Figure 7-6. A CELLSRV process in the Oracle Exadata Storage Server Software scans data blocks in each cell into memory and identifies only the rows and columns that provide valid results for the query. These results are returned from the Exadata Storage Server cells to the database server nodes in a constant flow of data that matches the predicates. There, the database consolidates the results and returns them to the client. This technique has

1. Check the database for any messages. 2. Create a ListAdapter from the results of this query and display them to the ListView. 3. Create a ChatSession to the address in the EditView and send your message text.

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Refsum disease is discussed with the hereditary polyneuropathies (page 1157). The Bassen-Kornzweig syndrome has its onset more often in late than in early childhood and is more appropriately described in the following section of this chapter. Ataxia-telangiectasia is described below. Galactosemia has been described on page 802 and Friedreich ataxia on page 949. Generally, it is not dif cult to differentiate these diseases from the acquired postinfectious variety that occurs predominantly in children. Ataxia-Telangiectasia This disease, sometimes referred to as the Louis-Bar syndrome, was rst described by Sylaba and Henner in 1926, long before Louis-Bar s report in 1941. It combines a progressive ataxia with humoral immune de ciency and telangiectasias. Like xeroderma pigmentosum and the Cockayne syndrome, ataxia-telangiectasia has been attributed to defective repair of DNA. The inheritance pattern is autosomal recessive. The disorder rst presents as an ataxic-dyskinetic syndrome in children who appear to have been normal in the rst few years of life. The onset of the disease coincides more or less with the acquisition of walking, which is awkward and unsteady. Later, by the age of 4 to 5 years, the limbs become ataxic, and choreoathetosis, grimacing, and dysarthric speech are added. The eye movements become jerky, with slow and long-latency saccades, and there is also apraxia for voluntary gaze (the patient turns the head

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by status epilepticus and trauma Some patients recover within a few weeks, but others require several months, and relapse during another drinking spree occurs frequently Restoration of motor power is attendant upon muscle regeneration but may be complicated by polyneuropathy and other syndromes of neuromuscular disability associated with alcoholism Haller and Drachman have produced rhabdomyolysis (with elevated CK and myoglobinuria) in rats by subjecting the animals to a brief fast following a 2- to 4week exposure to alcohol, suggesting that a similar mechanism may be operative in alcoholic individuals Perkoff and his associates described what is presumably a third form of acute muscular disorder in alcoholics, characterized by severe muscular cramps and diffuse weakness, occurring in the course of a sustained drinking bout.

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They noted a number of biochemical abnormalities in these patients as well as in asymptomatic alcoholics who had been drinking heavily for a sustained period before admission to the hospital elevated serum levels of CK, myoglobinuria, and a diminished rise in blood lactic acid in response to ischemic exercise, as occurs in McArdle disease In distinction to the latter, however, myophosphorylase levels were not consistently reduced in the alcoholic patients From time to time one observes in alcoholics the subacute or chronic evolution of painless weakness and atrophy of the proximal muscles of the limbs, especially of the legs, with only minimal signs of neuropathy in the distal segments of the legs and feet Cases such as these have been referred to as chronic alcoholic myopathy, implying a direct toxic effect of alcohol on muscle, but the data are insuf cient to warrant such an assumption.

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above), there has been described a rapidly progressive form of more widespread degeneration of the spinal cord (Mancall and Rosales) The myelopathy is characterized by a rapidly ascending sensorimotor de cit that terminates fatally in a matter of weeks There is a roughly symmetrical necrosis of both the gray and white matter of most of the cord This necrotizing myelopathy is distinctly rare, being far less common than compression of the spinal cord from cancer and even less frequent than intramedullary metastases Indeed, the status of necrotizing myelopathy as a remote effect of carcinoma is uncertain Henson and Urich have drawn attention to another rare spinal cord disorder usually associated with carcinoma of the lung This takes the form of large, wedge-shaped necrotic lesions scattered throughout the cord, affecting mainly the white matter of the posterior and lateral columns The clinical correlates of this disorder are also unclear.

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